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Potential Mechanisms of Mucin-Enhanced Acinetobacter baumannii Virulence in the Mouse Model of Intraperitoneal
Greg Harris1, Bruce E Holbein2,3, Hongyan Zhou1
1Human Health Therapeutics Research Center, National Research Council Canada, Ottawa, Ontario, Canada.
Abstract:
Porcine mucin has been commonly used to enhance the infectivity of bacterial pathogens, including Acinetobacter baumannii, in animal models, but the mechanisms for enhancement by mucin remain relatively unknown. In this study, using the mouse model of intraperitoneal (i.p.) mucin-enhanced A. baumannii infection, we characterized the kinetics of bacterial replication and dissemination and the host innate immune responses, as well as their potential contribution to mucin-enhanced bacterial virulence. We found that mucin, either admixed with or separately injected with the challenge bacterial inoculum, was able to enhance the tissue and blood burdens of A. baumannii strains of different virulence. Intraperitoneal injection of A. baumannii-mucin or mucin alone induced a significant but comparable reduction of peritoneal macrophages and lymphocytes, accompanied by a significant neutrophil recruitment and early interleukin-10 (IL-10) responses, suggesting that the resulting inflammatory cellular and cytokine responses were largely induced by the mucin. Depletion of peritoneal macrophages or neutralization of endogenous IL-10 activities showed no effect on the mucin-enhanced infectivity. However, pretreatment of mucin with iron chelator DIBI, but not deferoxamine, partially abolished its virulence enhancement ability, and replacement of mucin with iron significantly enhanced the bacterial burdens in the peritoneal cavity and lung. Taken together, our results favor the hypothesis that iron at least partially contributes to the mucin-enhanced infectivity of A. baumannii in this model.
Insights
Porcine mucin enhances Acinetobacter baumannii infection in mice. Iron in mucin appears to be a key factor in this increased bacterial virulence, suggesting new therapeutic targets.
Area of Science:
- Microbiology
- Immunology
- Infectious Diseases
Background:
- Porcine mucin is known to increase bacterial pathogen infectivity in animal models.
- The precise mechanisms behind mucin-mediated enhancement of bacterial virulence remain largely unelucidated.
Purpose of the Study:
- To investigate the mechanisms by which porcine mucin enhances Acinetobacter baumannii virulence in a mouse model.
- To characterize bacterial replication, dissemination, and host innate immune responses during mucin-enhanced infection.
Main Methods:
- Utilized a mouse model of intraperitoneal mucin-enhanced Acinetobacter baumannii infection.
- Assessed bacterial burdens, inflammatory cell recruitment (macrophages, lymphocytes, neutrophils), and cytokine responses (Interleukin-10).
- Investigated the role of iron by using iron chelators and iron replacement.
Main Results:
- Mucin significantly increased Acinetobacter baumannii tissue and blood burdens.
- Mucin induced significant neutrophil recruitment and early Interleukin-10 responses, but macrophage depletion or IL-10 neutralization did not affect enhanced infectivity.
- Iron chelation partially abolished mucin's virulence enhancement, while iron supplementation alone increased bacterial burdens.
Conclusions:
- Iron present in mucin is a significant contributor to the enhanced infectivity of Acinetobacter baumannii in the studied mouse model.
- Findings suggest that targeting iron availability could be a therapeutic strategy against mucin-enhanced bacterial infections.
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